R C 







LIBRARY OF CONGRESS. 



Shelf J»-X-l- 



UNITED STATES OF AMERICA. 




ORIGINAL INVESTIGATIONS 



IN 



DIPHTHERIA AND SCARLET 

FEVER, 

SHOWING THEIR KINSHIP AND CAUSE TO BE THE 

MUCOR MALIGNANS, 

{A Fungus in the Exudations , Blood, Urine and Sputum,) 



CURED BY QUININE TOPICALLY ADMINISTERED IN POWDER ON THE TONGUE, 

AND B Y INHALA TION. 



/ 

JAMES H. SALISBURY, B. N. S., A. M., M. D., 

MEMBER PHILOSOPHICAL SOCIETY OF GREAT BRITAIN, OF AMERICAN ANTIQUARIAN SOCIETY, AMERICAN ASSOCIATION FOR THE 
ADVANCEMENT OF SCIENCE, VICE-PRESIDENT WESTERN RESERVE HISTORICAL SOCIETY, 
. ft AUTHOR PRIZE ESSAY ON MALARIA, 1882, ETC. 



All rights reserved. Reprint Gaillard's Medical Journal, May, 1882. 




DETROIT : 

GEO. S. DAVIS, Medical Publisher. 
1883. 




- I 



it 



DIPHTHERIA AND SCARLET FEVER. 



Microscopical investigations connected with the exudation and expectoration of Angina 
Membranacea, Angina Maligna or Gangrenosa, and Scarlatina Anginosa; resulting in the 
discovery of the source of and the pathological process by which the exudations are pro- 
duced, and the further discovery of a peculiar species of Mucor developing in the diph- 
theritic membranes of Angina Maligna and which appears to be the true cause of the 
disease; with some remarks on treatment. 

Also some general conclusions on the artiology of fevers ; the peculiar functions of 
the epithelial systemic cell envelope; and the probable way in which the system receives a 
more or less permanent protective immunity, by one attack of certain contagious diseases 
against a second invasion of the same. 

M. Bretonneau gave to Angina Membranacea the name of Diphtheritis, on 
account of the pellicle-like exudations. The ordinary sites of these exudations, as is 
well known, are the fauces and pharynx; often, however, they extend past the pharyn- 
geal and laryngeal regions far down the oesophagus, and into the trachea and bronchial 
tubes, and even upward into the nasal fossae. 

Microscopic examinations show, further, that there is a tendency also for the 
lining membranes of the genital organs, intestines and bladder, and in short the epi- 
thelial cells of the entire mucous surface to take on the diphtheritic action. This 
renders it evident that this disease, like Scarlatina Anginosa (which it will be shown 
to resemble), is systemic, with a marked tendency to localization in the respiratory tract. 

Angina Maligna, in its worst form, accompanied by Angina Membranacea, became 
epidemic during the months of October, November and December of the year 1862, 
and January and February, 1863, over a tract of country, about five miles long from 
north-west to south-east, and three miles wide, situated from two and a half to five 
miles southwest and west of the city of Lancaster, Ohio. 

It first appeared immediately after a snow storm (the first of the season in 
October). The snow fell about two inches deep, upon a remarkably dry, parched soil, 
and was the beginning of the fall wet weather, after a long period of drought, which 
was so severe that it was impossible for the farmers to plow their soil for putting in 
the winter wheat. The grasses of pastures and meadows were parched, dry, and 
mostly dead; and the herbaceous plants of the fields and forests were in the same 
condition. The disease first made its appearance at the south-east end of the section 
before described, among the dry, sandy hills, and gradually progressed to the north- 
west. It exhibited, often in the same family, all grades of severity from a mild type 
of Angina Membranacea to the most severe form of Angina Maligna; where the 
extremities would become gangrenous, in some cases, several days before death. The 
malignant form was unusually fatal and rapid in its progress; often from two to five 
persons dying in a single family, within a few days of each other. The young became 
the victims, while those above twenty-five usually escaped. 

The section over which this malignant disease prevailed, composed of hills and 
high table lands, is abundantly supplied with fine springs of cold, free stone water, 
and is regarded as a particularly healthy region. It is inhabited mostly by sober, 
industrious German farmers. 

An excellent opportunity was here offered for studying the disease. Through 
the kindness of Doctors Effinger, Boerstler and Lewis, I was able to obtain the best 
of material for examination. 



DIPHTHERIA AND SCARLET FEVER. 



From its progress in this region, from family to family, and from other circum- 
stances, hereafter mentioned, there appeared to be no doubt of its contagious character. 
The period of incubation ranged, in different cases, from three to six and eight days; 
unless, accidentally, the air passages became directly inoculated with the virus or vege- 
tation, in which case the disease would begin to show itself immediately. 

The cases could be nearly all traced to exposure to the contagion of the dis- 
ease. When it once made its appearance in a family, any of the younger members 
seldom escaped. 

Before entering upon a description of the following cases, and the microscopic 
examinations of the exudations, etc., I will briefly narrate the characters of Angina 
Membranacea and Angina Maligna, set forth by Dr. Tweedie; as his remarks upon 
these diseases, in several important particulars, point in the direction of the results of 
these investigations. 

In speaking of Angina Membranacea, he says: "The patches are of various 
extent; in mild cases, white and ashy, separate, and presenting the appearance of super- 
ficial sloughs, for which they have often been mistaken; in others, dark colored, coa- 
lescent, and forming one uniform crust. The exudations may extend far down the 
oesophagus, or into the larynx, trachea and bronchise, and upward into the nasal fossae. 
The membrane beneath and between the pellicles is in some cases of a bright red, 
and in others purplish or livid. The exudations vary in density, from that of coag- 
ulable lymph, to that of soft pultaceous matter." 

" The local sensations are similar to those of Angina Diffusa, with the addition 
of that produced by irritation and obstruction of the air passages, when the disease 
has extended in that direction. It is common also for the sub-maxillary and cervical 
glands to become inflamed and tumefied. 

" The general symptoms are those of fever, and vary with the type of the latter 
and the degree of the inflammation. Where the patches are but few and circum- 
scribed, the disease is often called Ulcerated Sore Throat, such as may be seen in 
Scarlatina Anginosa, but there are no ulcers in these cases, for on removing the pelli- 
cles or sloughs, as they are called, we find the membrane beneath quite free from any 
other disorganization than the loss of its epithelium. In the worst cases, the pellicles 
are discolored by the admixture of bloody exudation and vitiated secretions of the 
throat, so as to create an impression that the parts are in a state of sphacelus. 

"These casts correspond to the Angina Maligna of others; but we have the 
united testimony of Bretonneau, Guersent, and Deslandes, formed on extensive micro- 
scopic observations, that there are no true eschars in these cases. The idea of gan- 
grene existing has been further kept up by the discharge of serous and fetid matter 
from the nostrils, and by the putrid character of the fever. Instances of this descrip- 
tion are very rarely met with, excepting when the disease prevails as an epidemic. 

" From the above, it appears that Angina Membranacea occurs in two forms. 
In one the local affection bears the marks of active inflammation, in the bright hue 
of the mucous membrane, and in the white, circumscribed exudations, unmixed with 
blood or sanies. 

"The constitutional symptoms in this form are likewise sthenic, the pulse being 
full and firm, the skin warm, and the nervous system — though disturbed — not exhib- 
iting the prostration so common in typhoid forms. The other variety may well be 
called Angina Maligna. 

"Its approach is often insidious, being attended with little pain or disturbance 
in the throat till the false membrane is already extensively formed, then the dysphagia 
becomes extreme; liquids are forced back through the nostrils, and symptoms soon 
occur denoting that the air passages are obstructed; such as a croupy cough, hoarse- 
ness and stridulous breathing. 

" The feeling of suffocation accompanying these symptoms is in part owing to 
the swelling of the lymphatic glands. On inspection of the throat, we see a thick 
pellicle, sometimes dense, not unfrequently pultaceous, variously colored, according to 



DIPHTHERIA AND SCARLET FEVER. 



the degree of its decomposition, or to the accompanying secretions, and either continu- 
ous or interrupted by fissures which exhibit the livid hue of the membrane beneath. 
The pulse is extremely rapid and feeble, delirium sets in early, and is soon followed 
by coma; and the collapsed face and sunken eyes indicate extreme exhaustion. Death 
often takes place suddenly from the laryngeal complication. 

" Bretonneau was led by the results of his dissections to attribute the death, in 
all the fatal cases, 10 the changes in the air passages. 

"As might be expected, a priori, the victims of Angina Maligna, are persons 
living in humid districts, where the disease is occasionally epidemic; among the inhabi- 
tants of crowded buildings, and the poor ill-fed classes of the community. 

" Persons, however, not under these depressing agencies, may be attacked by a 
severe form of the disease. Children are more liable to it than adults. Whether it is 
propagated by contagion is not absolutely determtned, but there are strong presump- 
tions in favor of this view. When the affection is epidemic, the difficulty of distin- 
guishing the operation of some generally diffused cause from that of contagion, meets 
us in this disease with the same force as in other epidemic maladies. The most un- 
exceptionable instances of contagion are those in which the sporadic form has been 
transmitted from one person to another. Guersent relates the case of a nun who 
caught the disease from a little girl whom she had nursed in the Hopital des Enfans, 
and he remarks that practitioners are frequently attacked after inspecting the throats 
of their patients. That the inflammation of the mucous membrane takes place in An- 
gina Membranacea cannot be denied, but why it should cause the secretion of coagu- 
lable lymph, rather than of serum and mucus, which are the ordinary products of 
mucous inflammation, cannot easily be explained. It is probable, however, that the 
peculiarity does not depend upon the local action merely, but upon the state of the 
constitution previously modified by epidemic influence. 

" In this disease there is frequently observed an erythematous or papular erup- 
tion on different parts of the body, and there can be little difficulty in arriving at 
the conclusion that it is a variety of Scarlatina Maligna.'" 

Dr. Tweedie further says " We are inclined to affirm that Scarlatina Simplex, 
Scarlatina Anginosa and the Scarlatina or Angina Maligna, and the sore throat, with- 
out efflorescence on the skin, are merely varieties of one and the same disease." 

REPORT OF CASES. 

The following communication contains a report of several well-marked cases of 
Angina Maligna which were attended and reported by Dr. Effinger: 

Dear Doctor : At your request, I have kept a careful record of the follow- 
ing well-marked cases of Angina Maligna, from which I have sent you, from time to 
time, as the disease progressed, samples of blood, urine, exudations and sloughs. 

Case I. — Amos Bear, a strong, healthy young man, aged seventeen, was taken 
down December 4, 1862. 

Thursday morning, December 4, he felt so badly that he remained in bed and 
ate no breakfast or dinner. Towards evening he vomited, felt pain in throat, neck 
swelling rapidly, externally. Sent for me about dark ; could not see him that even- 
ing ; prescribed a cathartic and foot bath, and flannel cloths wrung out of hot vinegar 
and sprinkled with salt, to be applied about the neck. 

Friday, 10 a. m., December 5, made my first visit; found him in bed, face 
anxious and look depressed ; pulse 92 ; not much fever or heat of skin ; back and 
side of neck much swollen ; more cedematous than glandular. 

On examination of throat, discovered a large diphtheric patch, one inch in diam- 
eter and oval in shape, on left tonsil. It had a dark, ashy appearance, was of soft 
consistence and easily penetrated, with well-defined edges; breath offensive, with a sickly 
meatish smell. The right side of the throat was deeply infected, engorged to a pur- 
plish hue, with a slight bloody exudation from a small surface posterior to the tonsil. 



DIPHTHERIA AND SCARLET FEVER, 



Continued external applications, and left chlorate of potash to be taken internally 
every four hours and used as a gargle. 

Saturday, 12 m., Dec. 6. — Pulse 92. General symptoms same as yesterday; no 
change in slough on left side ; some lumps of putrid matter, separated with difficulty 
by a spoon-handle ; fetor of breath more decidedly putrid than before. On the right 
tonsil, a well-defined diphtheritic exudation had made its appearance, three-fourths of 
an inch in diameter, closely adherent, but the edges could be slightly raised. The 
purplish engorgement not quite so distinct as yesterday. Continued treatment, with 
addition of mur. tinct. iron, and a more liberal diet. 

Sunday, 1 p. m., Dec. 7. — Patient not so well ; had a bad night ; forehead hot, 
pulse 92 ; more lassitude than before. Fetor of breath intolerable, decidedly putrid. 
Slough on left side about the same ; dark fetid shreds removed, showing considerable 
depth of slough. On the right side, the diphtheritic patch was much increased in 
size, oblong in shape, extending below the tonsil as far as could be seen. It is much 
thicker than yesterday, of a whitish yellow color and more adherent. The mucous 
membrane on its edge still of a dark, livid color ; obtained a sample of his morning 
urine, and the hawking expectoration produced by my examination, which I sent you. 
Applied wash of nitric acid, diluted two-thirds, freely, to both sides ; general treatment 
continued, with iron omitted. 

Monday, 4 p. m., Dec. 8. — Had a very comfortable night ; feels better; pulse 
86 ; no heat of skin ; fetor of breath not so offensive ; slough on left side evidently 
arrested ; dead lumps easily detached. On the right, side, the tripe-looking membrane 
has extended over the dark, livid border of yesterday. 

It now has an oval shape, and is larger than the slough opposite ; its lower 
edo-e well defined a short space below tonsil. Edges closely adherent ; cannot yet be 
detached by* gentle force. Took from arm i-j ounces of blood for examination, which 
I sent you, with some sloughs from fauces and a sample of his morning urine. Ap- 
plied freely the nitric acid, and commenced the iron again. 

Tuesday noon, Dec. 9. — Amos not so well to-day; pulse 100 ; forehead too 
warm ; neck still much swollen in front, as well as on sides ; pulse rapid, feeble, and 
not of much force ; poison evidently telling on the general system ; throat same as 
yesterday, except on the right side, where, under the diphtheritic exudation, there is 
apparently a large slough ; tried to separate it, but the least touch made the exposed 
surface bleed, and I discontinued my efforts. After a slight laxative, bowels being 
constipated, ordered quinine and iron, with nourishing food. I used no topical appli- 
cations, except chlorinated soda and potash. 

Wednesday, 12 m., Dec. 10. — Amos has less fever; pulse 92 and feeble; face haggard, 
and I do not like the expression of his eyes; continued the quinine and mur. tine, 
iron, with liberal diet. The slough on left side is clearing somewhat, but still looks 
badly. The left side is perfectly foul and ragged. I detached a portion that was 
loose, which I sent you in the bottle, I believe, on Saturday. I detached a few 
shreds from this side, and sent them to you between glass slides. You can readily 
distinguish them by their dirty-white appearance and tripe-like consistence, being 
tougher than the porous soft lumps from the left side. In the bottle you will also 
find some soft matter that I scooped with a spoon-handle from immediately under the 
exudated membrane. 

Thursday, 3 p. m., Dec. nth. — Amos has had a bad night. The diphtheritic 
exudation has appeared on uvula and palatine arch, on the right side. They are 
much swollen, and render deglutition very difficult. He drinks with great difficulty even 
water; most of it comes back through his nose. 

It is evidently spreading upward, and is in the nasal fossae. No difficulty yet 
in breathing. I obtained his morning urine and some expectoration, and matter from 
throat, which I sent you. I also sent you a large bottle of water from the Bear Spring. 
Pulse 96 and feeble. 

Friday noon, Dec. 12th. — Amos is worse, prostration more apparent; difficulty 



DIPHTHERIA AND SCARLET FEVER. 



of swallowing increased ; the respiration more labored, and I fear the diph- 
theritic exudation has reached the bronchi; pulse ioo, and feeble. The diphtheritic 
membrane is covering the velum palati and the arches to-day, for the first time. 

I penciled the edge with nitrate of silver, hoping to arrest the spreading. 
Neck, back of ears, and half way down very much swollen, and just above the sternum 
very cedematous. 

Saturday 10 a. m., Dec. 13th. — The diphtheritic exudation has traveled beyond 
the penciled caustic mark. 

The specimen I send you to-day speaks for itself. You see the dark line; all be- 
yond has spread since yesterday noon. 

This specimen was taken from the uvula. Amos is sinking; respiration still more 
labored, and deglutition impossible. You can hear his labprous breathing all through 
the house. Under the separated exudation from the uvula, there is no slough, simply 
a raw bleeding surface. The swelling pf the neck noticed yesterday has to-day almost 
entirely disappeared. 

Sunday 10 a. m., Dec. 14th. — Amos is still living, respiration becoming more 
and more difficult. Asphyxia is creeping on slowly but surely. Obtained a sample of 
morning urine which I sent you. 

Monday, Dec. 15th. — Amos died at 1 p. m. Death painful. Died of suffoca- 
tion. Exudation extends into bronchi, and probably into pulmonary air cells. 

Case II. — Nancy Bear, sister of Amos, aged 21. For some months prior to 
her brother's illness, Nancy was absent from home, visiting relatives, some twenty 
miles distant. On Saturday, Dec. 13th, the family sent for her, and she came home 
on horseback, the evening of the same day. Though much fatigued, she hung over 
her gasping brother that whole night. She was constantly about him till he died, giving 
way very much to her feelings. She became completely prostrated on Monday; fainted 
at the church on Tuesday morning at the funeral, and had to be carried home. I was 
sent for Tuesday afternoon. 

Nancy is a heavy, thick-set girl of leucolymphatic temperament; general health 
good. I saw her about dusk. Found her nervous and prostrated, but with no tangible 
disease, except a severe coryza affecting nasal cavities and frontal sinus. I advised salt 
water pediluvium, and a cathartic at bed time. 

Wednesday, Dec. 17th. — Was called again to see her. Complained of soreness 
about the neck and throat. Both nostrils were completely stuffed up with ropy mucus, 
and the throat so filled as to interfere with the examination of parts, but being 
removed, no sign was seen of diphtheritic exudation; but the next day, Dec. 18, 
after a careful swabbing out of the throat, I detected a slight pearly exudation on the 
left tonsil. 

Friday, Dec. 19th. — The symptoms about the same as yesterday. 

Saturday, Dec. 20th. — Was much improved, the nasal catarrh being the prominent 
symptom, and the white adherent exudation not increasing. Nancy was sitting up, was 
cheerful, and said she was much better. 

Her beau called to see her as usual, Saturday night, and she imprudently remained 
up with him most of the night. 

Sunday, Dec. 21st. — Was sent for. Found her much worse, the tonsils and 
velum were swollen and red, swallowing difficult, the voice hoarse and the breathing 
labored and painful. Auscultation of left lung gave the sibilant rhonchus. Clearly 
was it evident that the catarrh of the nasal passages had crept down into the trachea 
and lungs, and that the whole mucous membrane of the air passages was now in- 
volved. Still there was no increase of exudation in the throat beyond the slight patch 
on the left tonsil. 

Monday, Dec. 22d. — Had a restless night. On raising the velum, evidence of 
diphtheritic patches were seen on the fauces, high up. The nostrils were filled with mem- 
brane, but not easily detached. 

Tuesday, Dec. 23d. — With my polypus forceps, I detached specimens from 
both nostrils, one-eighth of an inch thick, which I sent you. In the throat it was 



DIPHTHERIA AND SCARLET FEVER. 



only too apparent, both in fauces and on tonsils; in appearance, white, glossy, thin and 
closely adherent, but in patches. It never became continuous though she lived for a 
week longer. 

Wednesday. — Disease gradually progressing. 

Thursday, Dec. 25th. — Obtained some blood from Nancy's arm; the blood flowed 
directly into the smaller bottle. The blood, in larger bottle flowed into a saucer, 
and after standing for a short time, was poured into the bottle. Obtained also some 
membrane from throat and nose, with some freshly expectorated mucus, which was 
sent to you. 

Friday, Dec. 26th. — Nancy is about the same as yesterday. 

Saturday, Dec. 27th. — Nancy appears to be improving and there is some hope that 
she may recover. 

Sunday, Dec. 28th. — Worse than yesterday; very weak; breathing labored, and 
pulse rapid and feeble. The exudations have extended into the tracheal and bronchial 
passages. From this time, the breathing grew more and more labored, until she died 
asphyxiated, like her brother Amos, on the night of January 1st, 1863. 

Case III. — Jesse Bear, brother of Nancy, a fine healthy boy aged 8 years, was 
taken down Dec. 22d, '62. 

Dec. 25th. — Jesse very sick, has a large diphtheritic exudation on each tonsil. 

Dec. 27th. — Large and extensive exudations, but very little constitutional dis- 
turbance. Obtained his morning urine and some of his expectoration, which I sent 
you. Jesse continued to fail and the exudation to pass lower and lower into the 
trachea and bronchi, till, on January 6th, he expired as did his brother Amos. 

Case IV. — Peter Bear, brother of Jesse, a strong healthy boy of 12 years, was taken 
down with the disease, Dec. 25. 

Dec. 27. — Fever very high; exudation on right tonsil; vomited while 1 was pencil- 
ing his throat; a sample of vomited matter I sent you; Peter's case was one of simple 
Angina Membranacea and did not terminate fatally. There were three other cases in 
this family. Mrs. Bear, who had a slight attack; Susan, a young daughter, and a little 
grand-daughter, all of whom recovered. The only persons escaping were Mr. Bear and 
his eldest son aged about 23. 

Yours truly, 

M. Effinger. 
Dr. J. H. Salisbury. 

From Dr. Effinger's report it will be seen that out of seven cases in the Bear 
family, three died and four recovered. In almost every instance, when Malignant 
Diphtheria [Angina Maligna) appeared in a family, it was equally, if not more fatal. 
In support of this fact, we will mention briefly the following instances: 

Mr. Bailor had six children, and one grandchild, all of whom had Diphtheria. 
Four died, and three recovered. Of the four that died, three were females, and one 
male; they were respectively three weeks, seven, eleven and twenty years of age. Of 
those that recovered, one was the married daughter who had but a mild attack of 
Angina Membranacea. The ages of the two others were respectively thirteen and 
fifteen years. Of the daughter aged eleven, who died, one leg became gangrenous 
to the knee several days before death. One foot of the boy aged seven was very 
much swollen and also finally became gangrenous before death. Dr. Lewis attended 
this family. 

In the Sandris family the mother and all the children, six in number, had the 
disease. The mother and four of the children died, so that out of seven cases in 
this family, only two recovered. 

In Mr. Karn's family out of four children that had the disease three died. 
Their ages were respectively five, eleven and fourteen. A grown daughter, aged about 
twenty-one, and a nursing infant escaped without taking the disease. Dr. Lewis 
attended this family. In two of these cases, the feet and legs up to the knees 



DIPHTHERIA AND SCARLET FEVER. 



became pulseless and cold twenty-four hours before death, and there was a disposition 
to gangrene. 

In the Brooks family, all of his children, three in number, had the disease, two 
recovered and one died. In Warren Stripes's family, two grown daughters, the only 
children at home, had the disease. One recovered and one died. The first one taken 
down, four or five days previous to the attack, visited Mr. Bailor's family, and helped 
to " lay out " one of his children that had died of the disease. 

In Mr. Himes's family the mother and one child only had the disease. The 
former recovered and the latter died. 

In Mr. McCabe's family, all the children, six in number, had the disease, and 
all recovered. 

From the foregoing statements, it will be seen that out of thirty-eight cases, 
there were eighteen deaths, and twenty recoveries. Many of those that recovered, 
had merely the membranous type of the disease. This, however, will represent about 
a fair average proportion of the recoveries and deaths in those attacked with the 
disease, in the district previously mentioned, where malignant Diphtheria prevailed. 
But few families in the district were exempt from the invasion. 

Since writing the foregoing, I have received the following letter from Dr. Lewis, 
in which are reported two interesting cases of Angina Maligna or Gangrenosa. 

Lancaster, Ohio, April 3d, 1863. 
Dr. Salisbury — Dear Sir: — Your letter asking for a report of cases of Diph- 
theria has been received. In referring to my notes of cases, I find that the epidemic 
which ravaged the south-west part of our county, made its advent on the 19th day 
of October, 1862. Two children were attacked simultaneously in the same family, 
one aged nine and the other eleven years, one male and the other female. These 
cases had progressed for four days, before I was called to see them. I cannot, from 
personal observation, state the mode of the attack, but at my first visit I found the 
elder (a girl), with a quick, feeble pulse, cold extremities; shrunken, pale and 
agonized countenance; unable to articulate; the parotid and submaxillary glands enlarged; 
the tonsils enlarged; the uvula elongated and of an ashy appearance; the tonsils on 
the right side covered with a dark fetid slough, surrounding which was an areola of 
an ashy appearance, beyond which the parts presented a dark cherry color, gradually 
disappearing. The case terminated fatally in about six hours after I saw her. 

The boy was in about the same condition, but had a less aggravated form of 
the disease. He recovered. These two cases appeared to be the nucleus from which 
the disease spread; mostly in a north-west direction, choosing the slopes of the hills 
and high table lands, rather than the summits and valleys. 

This disease in its progress presented two distinct forms; the first, the most 
usual, was what I have termed the malignant or typhoid. This form was ushered 
in by a low, quick pulse, a dry harsh condition of the skin, a feeling of fullness 
and uneasiness in the head (not amounting to headache), dry tongue, great thirst, 
the parotids and glands of the neck on about the second day becoming sore to the 
touch, the muscles of the neck at the same time becoming stiff, the tonsils, pharynx 
and uvula assuming a dark cherry or purple hue. In from six to twelve hours, a 
small yellowish-gray spot would make its appearance upon one or both tonsils, about 
the size of a grain of wheat. This spot had the appearance of an erysipelatous 
blister, which would spread rapidly and burrow deeply, assuming a dark-brown or 
black hue, and forming in a few hours a fetid siough, which would, in the course 
of from thirty-six to forty-eight hours, begin to break down. 

The condition of the skin remaining the same, the pulse becoming weaker, the 
strength failing rapidly, the pupil of the eye enlarged and vision partially lost, so 
that small objects could not be seen, and the disease often terminating fatally in from 
four to seven days. 

The other form I have taken the liberty of calling the inflammatory, to dis- 
tinguish it from the typhoid form; its mode of attack being entirely different. Coming 



8 DIPHTHERIA AND SCARLET FEVER. 

on with full, hard, bounding pulse, congested state of the capillaries, high fever, 
headache, nausea, sometimes vomiting, the tongue coated with dark-brown fur, the 
throat assuming a clean bright scarlet hue, the exudation making its appearance about 
the second day, and having the appearance of milk curd of a clear white cheesy 
character, easily broken down. This form was readily amenable to the ordinary 
treatment. No death occurred from such attacks, in my practice, which during the 
winter was extensive, for I treated over one hundred cases from October, 1862, to 
February, 1863. A more detailed account of the following cases may be of interest: 

Case i. — Male, aged n. Attacked November 6th, and, from all I could learn, it 
appeared to be at first a mild form of the malignant type of the disease. I did 
not see the case till some four weeks after the attack. This with the succeeding 
case (2), was of much interest. The child was laboring under a low grade of fever, 
dry, husky skin, loss of appetite, partial vision, tenderness of abdomen, periods of 
intense suffering occurring every two, three or four hours, which he attributed to a 
sore on his foot from which the skin had been rubbed by the shoe. Upon exam- 
ining the sore, I found the extremity cold, the ulcer about the size of a dime, with 
a shrivelled bluish elevated border, the centre of a dark fetid slough, without any 
appearance of granulations, having much the appearance of a chancre. The ulcer 
continued to increase in size, the foot assuming a mottled appearance. Soon the 
toes began to shrivel about the nails, dry gangrene made its appearance, soon invad- 
ing the whole foot; the brain became implicated, and the patient rapidly sank. 

Case 2. — Aged 13, sister of Case 1; attacked about the same time, and, from what 
I could learn, in the same manner. I was unfortunate in not seeing this case until 
the lapse of about four weeks. When I did see the patient, found her in about 
the same condition as Case 1 at my first visit. After treating the case for some 
days, the ulcers in the throat gradually healed, but the powers of life were far 
spent. Like her brother, she had upon her foot a sore caused by the chafing of 
the shoe. This sore was an ordinary one, showing considerable indisposition to 
heal, but an ordinary abrasion, till after the throat healed, when to my amazement 
a regular diphtheritic deposit made its appearance upon the sore, which rapidly 
passed into an ulcer with the same appearance that was presented in Case 1 ; 
refusing to granulate, and absolutely maintaining that cold, flatly malignant appear- 
ance of the chancre. This ulcer spread by a gradual death of the tissue, 
not rapid, but sure and persistent. In the course of ten or twelve 
days, gangrene showed itself upon the toes, gradually advancing until the toes 
were entirely involved. Mortification now made its appearance in the foot around the 
abrasion caused by the shoe, which spread slowly until it reached a point about three 
inches above the ankle joint, where a partial line of demarcation was formed, and 
gradually became more distinct for four days, but finally claimed more, and gangrene 
slowly continued up the leg until the whole member was involved, and the little 

patient was relieved from her sufferings. 

Very respectfully, 

J. W. Lewis. 

The two cases reported by Dr. Lewis, where gangrene attacked the extremities 
several days previous to death, are highly interesting. It appears that these two cases 
had lingered under the influence of the disease some four weeks previous to the first 
visit of the Doctor, and that gangrene did not set in till several days after. The 
diphtheritic exudation on the surface of the abrasion on the foot of each of these 
patients shows that the morbific cause had pervaded the entire system, and that it is 
capable of producing a gangrene in the extremities, similar to that which it causes in 
the original region of invasion. 

microscopic examinations of expectorations, exudations and sloughs in diph- 
theria. 

The exudations and sloughs herein examined were taken from the throat and 
fauces of Amos Bear, December 10th, the sixth day of the disease, and sent to me 



DIPHTHERIA AND SCARLET FEVER. 



on the same day by Dr. Effinger. The membranes had the usual appearance of 
diphtheritic exudations. With them was considerable expectoration or mucous secre- 
tion of the anginal region. 

The cells of this mucous secretion had a peculiar and interesting appearance. 
The minute cell contents appeared more distinct than in health, and in many instances 
were in active and independent motion, moving rapidly among each other and around 
the laro-e central nuclei. By carefully watching the mucous cells it was also discovered 
that thev, too, exhibited independent vitality, and had a slow progressive movement 
mostly in right lines, either singly or in whole columns or in masses. This motion 
was very slow, but by watching, in many instances, a single cell for hours together, its 
movements and general metamorphoses were fully and satisfactorily determined. The 
mucous cells of the spittle and expectoration, as is well known, are the products of 
the parent epithelial cells, lining the air passages, and those forming the secreting 
and organizing surfaces of the salivary system. These cells, in a normal or healthy 
condition, immediately after being formed, have the appearance as seen at a, s, and 

t, Fig. i, PL I. 

In the diphtheritic exudations and expectoration, these cells have taken on an 
increased tendency to be metamorphosed into filaments, each being provided with a 
minute hair-like appendage and possessing the power of independent motion. These 
diphtheritic mucous cells are seen at b, c, and h, Fig. i, PI. I. Their minute cell 
contents could be readily seen moving independently about among each other and 
around the central neuclei. As the vitalized mucous cells (b and h) gradually pro- 
gressed, it was found that the hair-like appendage gradually became larger and longer, 
till it could be seen to be a tube, into which a portion of the minute cell contents 
of the mucous cell passed, (c). This metamorphosis or filament development from 
cells gradually progressed till, after many hours, the cell entirely disappeared, having 
been spun into a filament like that seen at f, Fig. i, PL I. Sometimes from two 
to many cells would be seen united in a moniliform line, the cells of which would 
begin to separate, remaining connected by a filament as seen at d, e, and m, Fig. i, 
PI. I, and this separation would become greater and greater, until the entire string 
of cells would be metamorphosed into a long tubular filament containing in it a por- 
tion of the minute cell contents of the mucous cells. 

The only portions not metamorphosed into filaments were the large central 
nuclei. This operation of cell metamorphosis was watched day after day for several 
weeks, till I became fully satisfied that this general active filamentous development of 
the mucous cells was abnormal, and that from it resulted the membranous exudations 
of Diphtheria. It was satisfactorily determined that the diphtheritic membranes are 
formed by the rapid metamorphosis of the mucous cells into filaments, which process 
begins in this disease before they are fairly liberated from the mucous follicles, and 
even from the parent epithelial tissue. 

As the filaments are developed they become interwoven and thus form a more 
or less thick and compact adherent membrane, according to the activity of the secre- 
tion and the cell metamorphosis. The external surfaces of the exuded membranes 
have the appearance seen at r, and q, Fig. i, PL I. 

The filaments are so transparent, and their plastic walls become so blended with 
each other, that it is with difficulty they are distinguished after the membrane is fully 
formed. In its early stages, however, it can be readily resolved into its ultimate fila- 
ments, u, Fig. i, PL I, represents the two kinds of minute cells, highly magnified, 
that have independent motion in the mucous cells, b, c, and i, Fig. i, PL I. p, rep- 
resents the minute cells, highly magnified, seen on the surface of the fragments of 
exudation q, and r. g, are masses of sporidia of the sphaerotheca pyra — the species 
that produces blight in the apple, pear and quince trees and decay in their fruit, 
h, i, k, m, n, and o, Fig. i, PL I, represenl the mucous cells in the expectoration 
and exudations of Nancy Bear, in their various stages of metamorphosis. Many other 
cases have been examined, all of which go to confirm the views here advanced. 



DIPHTHERIA AND SCARLET FEVER. 



SLOUGHS OF ANGINA MALIGNA. 

The sloughs from the throat of Amos Bear were subjected to a careful micro- 
scopic examination. The bodies represented under Fig. 2, PI. II, were in the sloughs. 

Examinations of like sloughs from Mr. Karn's son and several others, revealed 
the same bodies with the single exception of the genus anguillula seen at a, PI. V, 
Fig. 6, which was only found in the sloughs of Amos Bear, and which probably came 
from some vinegar gargle he may have used. 

The minute forms represented at a, Fig. n, PI. II, are peculiar active bodies, 
which are really the spores of embryonic filaments of minute species of alga? or fungi. 
The parent gland cells of animals have the power of taking in and transmitting freelv 
the spores of this vegetation. All organic bodies are filled with these spores, which 
seem to be quiescent during the physiological states, but as soon as pathological con- 
ditions arise they develop and multiply with incredible rapidity. They become verv 
abundant during the fermentation and incipient decay of all organic matter, and espe- 
cially so in nitrogenized animal tissues. At b, c, d, Fig. 2, PI. II, are represented 
the mature algoid filaments, which are found in multitudes running in all directions 
through the exudations and sloughs. e, f, g, and h, Fig. 2, PI. II, are cells that 
have the appearance of being the spores and sporangia of the Mucor Malignans 
described further on; g, and h, are more highly magnified than e, and f; i, appears 
to be an ascus highly transparent and colorless, k and p, sporidia of the apple blight 
fungus (sphserotheca pyra), m, n, and o, sporidia, single and in mass of the sphasrotheca 
pyra, vegetating with mycelial filaments. These occur abundantly in the sloughs. They 
are present in large quantities in apple fruit this season and may be carried into the 
system through the apples eaten. This species of fungus appears to be poisonous to 
some vegetable tissues, and the sporidia excite irritation of the fauces, trachea and 
bronchi when inhaled. Another species Sphaerotheca persica (erysiphe graminis) produces 
the disease known as the "cirri and blister," in peach leaves, and which proves so deleterious 
and destructive to peach orchards. Its known deleterious effects upon vegetation, 
together with its tendency to irritate the pulmonary membranes when inhaled, renders 
it probable that it may have some influence in exciting disease in the human sub- 
ject. At b and x, Fig. 6, PI. VI, are represented two species of fungous filaments. 
These are found in the expectoration of diphtheritic patients this season. That repre- 
sented at x, occurs in vast numbers in ripe persimmons this year, in central Ohio. 
q, Fig. 6, Plate VI, represents a sample of numerous knots of mycelial filaments, 
that are highly transparent, scattered over the surface of the sloughs and patches of 
exudation. 

u, v and w, Fig. 2, PI. II, large mucous cells. 

Besides the bodies represented under Fig. 2, PI. II, there were numerous highly 
transparent, large and loosely formed filaments, single and in bundles, that had the appear- 
ance of the mycelium, c, e, Fig. 3, PI. Ill, of the Mucor Malignans. There were, 
however, no fertile threads. Strongly suspecting that these filaments were fungoid, 
after cutting off a portion of the slough for further microscopic examination, I placed 
the balance in a tightly corked two-ounce wide-mouthed bottle, and set it aside in a 
room where there was no fire. The temperature in this room ranged from 60 to 65 
F. In a few days after being set aside, a white mould or fertile thread began to 
appear on the surface of the slough. This mould gradually increased till on 
December 28th, it enveloped the entire surface with a mass of white fertile threads 
that resembled fine cotton. On examining this under the microscope, I found the 
surface fertile threads to emanate from the same mycelium as was noticed running 
all through the slough and exudation on Dec. 10th, when freshly separated. 

At that time, however, there were no signs of fertile threads, and the mycelium 
was very much more transparent and less firm than on December 28th. On placing 
this mycelium and fertile threads under the microscope, a most beautiful fungus in 
full fruit was exhibited, samples of which are seen at a, b, c, d, e and u, Fig. 3 
PI. III. d, represents the threads of the mycelium packed together and filled with 



DIPHTHERIA AND SCARLET FEVER. 



minute cells and granules, and covered often as at e, with minute cells. Mingled 
with the threads were numerous highly transparent spore-like bodies, that had no con- 
nection with them. This fungus appears to belong to the Genus Mucor. Not having 
met anywhere with a description of this species, I have named it the Malignans, as 
at this stage of the investigation it seems to have something to do as the cause of 
Malignant Diphtheria, as will more fully appear further on. 

a, represents a fertile filament bearing three grape-like clusters of sporangia. 
These bodies resemble mucous cells, and appear like the cells of diphtheritic exuda- 
tion and expectoration. The mycelium and minute cells are matted together in the 
exudation and sloughs of diphtheria, and covered with clusters of large cells, somewhat 
as seen at u, Fig. 3, PI. III. Often, however, the large cells are mostly absent. 

b, Fig. 3, PI. Ill, represents a fertile filament, covered with fruit or sporangias in 
an early stage of development, m, represents the minute cells highly magnified, that fill 
the large cells. 

g, n, s and t, Fig. 3, PL III, represent numerous active bodies moving about among 
the filaments, and which are seen at a, Fig. 2, PI. II. 

v, Fig. 3, PL III, represents the mature fruit after it has separated from the 
fertile threads. These cells are what I have found frequently in diphtheritic exuda- 
tion. They so much resemble mucous cells that they would readily be mistaken for 
them. I had supposed them to be mucous cells until I obtained the mature plants 
producing fruit. 

The minute bodies at w, Fig. 3, PL III, are what appear to be the spores of the 
Mucor Malignans. 

Diphtheria Produced by Inhaling the Spores of the Mucor Malignans. — On the 
28th of December, before opening the bottle containing the diphtheritic slough and 
exudation, covered with white mould, I locked myself in my room and opened the 
windows to prevent exposing the rest of the family to the disease. All the food I 
took for the next three days was hastily passed to me by my wife through the door 
slightly opened. 

I was determined to make careful microscopic examinations and drawings of the 
fungus, with full description of all the circumstances and conditions, no matter what 
might be the result to me. 

In removing the cork from the bottle, the slight jar sent the light spores out 
of the mouth of the bottle, appearing like the spores flying from a compressed "puff 
ball." These I freely inhaled. 

In a few minutes I had the vegetation under the microscope, and was making 
my drawings of the plant which are represnted in Plate III, Fig. 3. 

My throat and fauces began to get dry, hot and feverish, almost immediately 
after inhaling the spores. In less than thirty minutes, the same symptoms excited in 
the throat and fauces had extended down the trachea and bronchi, and seemingly into 
the air cells. With the dry, congested, hot feeling, was a heavy, persistent, dull pain, 
as if the parts affected were partially hepatized and useless. There was a feeling 
of oppression about the whole chest, and the breathing unsatisfactory and labored. 
These feelings became more and more intensified, so that in a few hours I was almost 
incapacitated from going on with the microscopic work and drawings. The spores had 
passed so freely and deeply into the air passages, and the oppression and irritation of 
the parts was so intensified, that I began to fear that I should not be able to pursue 
the investigation further, unless I could get relief. 

Believing the cause of my suffering to be the spores inhaled, I immediately 
began taking one grain of quinia sulph. every thirty minutes; and also to inhale and 
snuff an equal amount at the same time. In addition to this, I gargled a strong 
solution of tinct. ferri chloridi every time my throat became dry and sticky. In a short 
time the troublesome irritation in the throat, fauces and air passages began to be re- 
lieved, so that I was comparatively comfortable and able to go on with the microscopic 
work and drawings. 



DIPHTHERIA AND SCARLET FEVER. 



I am fully satisfied from what occurred during the attack and from my subsequent 
experience with the disease, that I should probably not have recovered if I had not 
treated myself heroically, as I did; for the mucous membranes of the entire air pas- 
sages were inoculated with the cause of the most malignant type of Diphtheria I have 
ever met with. 

The quinine, taken internally and inhaled every half hour, kept the system and 
surfaces so saturated with it that the vegetation could make but little headway, and con- 
sequently the disease was comparatively light and soon overcome. The disease was 
accompanied by a ropy, adhesive exudation, which excited hawking and spitting fre- 
quently. The same state extended down the oesophagus, and into the stomach and 
intestines. 

Bowels (which were before regular and in fine, healthy condition) became con- 
stipated, and feces hard and plastic. During the night there was considerable burning, 
heavy pain in stomach and bowels, aggravated by lying on the abdomen, and eased by 
lying on the back. There was scarcely any tenderness on pressure. Counter-irritation 
produced no relief. 

On the following morning, the first mucus that was coughed up contained many 
of the bodies v, and the spores w, Fig. 3. Plate III. Hawking to dislodge the ad- 
hesive mucus would excite hiccoughing, while but little matter would be raised. Cough- 
ing aggravated the pain. 

Dec. 30th and 31st. — All the symptoms were aggravated. On the 30th there was 
considerable fever, with a dry, hot, heavy, congested feeling of the whole mucous lining 
of the air passages and oesophagus, stomach and intestines. Urine became scanty and 
high-colored, and deposited a large sediment. There was a dry, pricking, constrict- 
ing feeling in the throat and fauces, with a sticking together of the part. The 
mucous secretions from the air passages and mouth were ropy and filamentous, and 
the mucous cells had the appearance seen at Fig. 1, Plate I. 

There was also pain in the sides of the neck, in the thyroid cartilage, and in 
the parotid and sub-maxillary glands. During the night, slept well. 

December 31. — The back part of the throat and fauces were covered with diph- 
theritic exudations. The mucous membrane of the air passages and digestive canal 
felt less congested and hot, and the secretions of the bronchi and fauces were less 
ropy, and had less tendency to pass into filamentous metamorphosis. Bowels less con- 
stipated. Urine still scanty and high colored, with a large sediment. 

1863. January 1. — Still better. The exudation patches in the throat are disap- 
pearing, and the secretions of the air passages less ropy, and bowels quite regular, 
appetite good. Continue the quinine sulph. every half hour. 

January 4. — Have been constantly improving since the first. The diphtheritic 
patches have entirely disappeared, and feel quite well except a heavy, aching pain in 
the laryngeal and pharyngeal region, with a slight difficulty in perfect articulation. 

This latter result is of frequent occurrence after recovery from severe attacks. 
Often this partial paralysis of the anginal region lasts for some days after recovery 
from the disease. 

A good illustration of the contagiousness of the disease occurred in this instance. 
Notwithstanding the precautions taken, about eight days aftCr the appearance of the 
first symptoms in my case, my wife was taken down with the disease. The only 
exposure she had was in passing the food to me through the slightly opened door, 
and this only for a moment, three times a day. Her attack was sudden and severe, 
and required energetic treatment to prevent the exudation from extending into the 
bronchi. Two days after her attack her sister was taken down, tind on the following 
day her brother. All recovered. 

Blood in Diphtheria. — The blood corpuscles of malignant Diphtheria are plastic 
and sticky, and have a peculiar tendency to adhere together, and to filamentous meta- 
morphosis, showing that the disease is not local but systemic, probably influencing and 
modifying the organizing functions of the parent cells of the lacteal and lymphatic 
systems and spleen — in short, the entire parent gland cell tissue. 



DIPHTHERIA AND SCARLET FEVER. 13 

At Fig. 4, Plate IV, are seen the various abnormal conditions and bodies of 
the blood of Angina Maligna. At a, and b, are seen masses of cells, resembling 
diphtheritic anginal cells. They are, however, colorless corpuscles formed by the spleen 
and the lacteal and lymphatic glands, and contain the micrococcus spores of the diph- 
theritic fungus. 

This peculiar tendency to stick together and become aggregated in irregular 
masses is abnormal. 

At c, c, Fig. 4, PI. IV, are thin, pliable sacks, constantly changing in shape, 
filled with minute, vitalized granules constantly in motion — protoplasmic. 

The sacks have an amceba-like motion, and communicate with the cavities of 
the cells b, and their contents are the minute cell contents of these cells, d, repre- 
sents these minute, independently moving granules, more highly magnified, e, a cell 
like those at i, and b, Fig. i, PI. I, having a hair-like appendage, it having taken on 
and commenced the process of filamentous metamorphosis, f, rhomboid epithelial cells, 
that are removed from their attachment and are floating in the blood, g, a large cell 
passing into a filament. At h and k, are represented algoid filaments that occur in 
little groups and skeins in the blood. 

Attached to the filaments k, are many spores of the vegetation. m 3 and n, are 
masses of fibrin, through and in which are seen algoid filaments, i, filaments resem- 
bling filamentous neurine. This kind of filament was frequently met with in the blood 
of Amos Bear. All these bodies occur abundantly in the blood, showing a formula- 
tive condition, and a disposition in its cells to become metamorphosed into filaments, 
and a tendency in these filaments to become aggregated in masses, forming clots. 
This explains why there is a disposition to gangrene — from a kind of embolism in 
this malignant form of the disease, the algoid spores, and filaments and spores, and 
the blood aggregating, forming masses, clots and emboli choking up the capillary ves- 
sels, so as to impede and in some cases entirely stop the circulation. 

Urine in Diphtheria. — The lining membrane of the urinary organs also takes 
on diphtheritic functional derangements. In all cases of Diphtheria, there is the same 
peculiar, flocculent, pinkish-white deposit, made up of minute granules of urates, like 
those at Fig. 5, PI. IV. With these are many crystals of lithic acid, often very large, 
and having the appearance of those seen at a, b, c, d and f, Fig. 5, PL IV. 

With these are frequently found cistine and the peculiar crystalline forms seen 
at e, d, and k, Fig. 5, PI. IV. 

Also epithelial cells and their products, undergoing the filamentous metamor- 
phosis, with many algoid filaments. 

At i, are represented crystals of the lithates of soda and ammonia, which fre- 
quently occur in diphtheritic urine, w, and v 1 , Fig. 7, Plate VI, represent peculiar 
mucous cells, ruptured by their minute cell contents escaping, q, and q 1 , Fig. 6, PI. V, 
spherical algoid cells uniting into moniliform filaments, g, fungoid filaments, h and 
1, the so-called vibriones, which are united into embryonic algoid or fungoid filaments, 
m and m', Fig. 6, PL V, algoid or fungoid filaments already formed, in which no struc- 
ture can be made out. t, u, v and w, Fig. 6, PL V, various stages in the formation 
of algoid filaments, from the so-called vibrio, r, and s, are highly magnified. 

The bodies here represented in diphtheritic urine, under Fig. 5, PL IV, are the 
result of careful microscopic examinations of the urine of twenty-three cases of well- 
marked Diphtheria. In one case that has come under my observation, through Dr. 
Effinger, the attending physician, the diphtheritic derangements were wholly confined 
to the bladder, it never producing any abnormal anginal conditions that were noticed 
by the patient. The patient was a married lady, this attack occurring while she was 
attending on her husband, who lay sick with ordinary Diphtheria (Angina Mem- 
branacea). 

Treatment. — During the twenty years that have elapsed since making these in- 
vestigations and preparing this paper, I have treated several hundred cases of Diph- 
theria with quinine sulphate and tinct. ferri chloridi, and I can only call to mind the 



14 DIPHTHERIA AND SCARLET FEVER. 

loss of a single case, and that was a German boy, who would not take the medicine 
with any regularity. The quinia sulphate should be given by the mouth, in powder, 
every half hour, keeping the mouth, fauces and throat constantly covered and saturated 
with it— also snuff and inhale it at the same time, so as to keep the surfaces of the 
entire air passages covered and saturated with it. 

In addition to this I have used the following as a gargle : 

IJ Tinct. ferri chloridi 3 j 

Aqua I vii j 

S. Gargle every hour. 

1^ Carbolic acid (cryst. white) 3 j 

Salicylic acid 3 ss 

Water § xii 

Pure glycerine | iv 

Ol. menth. pip gtt. xv 

S. Gargle every half hour before taking the quinia sulphate. 

The quinia sulphate is the remedy to be depended upon for checking the de- 
velopment of the case. 

There are many little things to be done to relieve and make more comfort" 
able, such as hop poultices around the neck, so covered in as to bring the steam 
from the hops up around the mouth, where it is inhaled. This often soothes and 
relieves the suffocating and croupy condition in children. The swallowing of small 
bits of ice often aids in loosening up the particles of exudation. 

Penciling the throat with alcohol also relieves the sufferings of the patient. 

If quinine cannot be obtained, any antiseptic remedy, or any medicine that will 
check or control the fermentation in a yeast-pot, or preserve meat from spoiling, 
will be useful in aiding the cure. Among these may be mentioned permanganate 
of potash, sulphites, all the mineral acids, salt, borax, benzoate of soda, potassium 
chlorate, salicylic acid, carbolic acid, tinct. ferri chloridi, bromine, iodine, sulphur, 
etc. 

In certain conditions where the cough is croupy, and the membranes tough, 
and expectoration adhesive and ropy, with a strong tendency for the disease to invade 
the trachea and bronchi, small doses of mercurial, often administered, check or con- 
trol this dangerous tendency, so that the exudations become softer, membranes less 
adhesive, croupy cough ceases, and the patient begins to improve. 

Scarlatina, the Symptoms and Derangements of; Similar to those of Diphtheria. — 
The mucous cells of the anginal exudation of Scarlatina, with the bodies found in the 
blood and urine, present marked similarities to those of Diphtheria. 

In both diseases there is a strong tendency for the cell products of parent 
epithelial cells to undergo filamentous metamorphosis. 

The disease in both cases appears to emanate from functional derangements in 
the organizing processes of the ultimate epithelial cells, and in part appears to result 
in a too rapid development of cells into filaments. The primary cause of both 
diseases, however, must consist in some morbific agent, which operates upon these 
cells, poisoning the nutrient products which they originate, so that after a certain 
limited period, which is the period of incubation, the whole system begins to sym- 
pathize, and take on a series of abnormal actions, which are simply systemic efforts 
to eliminate from the organism the morbific poison, and which actions constitute the 
symptoms or peculiarities of the disease. In this light the functional derangements 
in the organic processes of epithelial cells, become simply a resultant action excited 
by the primary cause of the disease, and are one of the efforts of nature to eradi- 
cate morbific matter, by accelerating normal changes in organic processes. 

It should therefore be the constant care of the physician, not to run counter 
to nature in her efforts to cure the disease, but simply to so equalize, aid and 
modify her actions, as to alleviate suffering and guard against dangerous results. 



DIPHTHERIA AND SCARLET FEVER. 15 

With these few preliminary remarks we proceed to the microscopic examination 
of the expectoration, exudation, blood, urine and the desquamated cuticle of Scarla- 
tina. 

Expectoration and Exudation. — The peculiar abnormal and similar tendency to the 
filamentous development of the mucous cells of the expectorated and exuded products 
of Scarlatina and Diphtheria, renders it evident that the anginal epithelial functional 
derangements in both diseases are remarkably similar. This similarity is found also 
to extend to the abnormal products of the blood and urine. This makes it conclu- 
sive that the same systemic, epithelial, functional derangements are common to both 
diseases. The results here obtained are confirmatory of Dr. Tweedie's supposition 
previously given. 

Fig. 7, Plate VI., represents the appearance of the mucous cells of the expec- 
toration and exudation of Scarlatina Angina. By comparing the filamentous meta- 
morphosis going on in these cells with that exhibited at Fig. i, PL L, a remarkable 
similarity will be noticed. 

a, Fig. 7, PI. VI., represents the normal mucous cell immediately after being 
formed and before it takes on the active condition, or begins to manifest independent 
activity, b, c and h, are mucous cells in Scarlatina, in the active stage. The most 
of the cells in this stage have a single fine caudal filament, resembling an extremely 
fine hair, tapering from the cell, and projecting from its posterior side, or from the 
side opposite to the direction in which it moves. Sometimes there are two or even 
three hair-like processes visible. The length of these hair-like processes in the early 
stages is usually from two to three times the diameter of the cell. 

The motion of these cells is a very slow, uniform, progressive one, often so 
slow that even an experienced eye would fail to detect it, unless the attention was 
called particularly to it, and the observations continued on the same cell often for 
hours. By selecting, however, a single cell standing alone, and keeping the eye on 
it for some time, a perceptible movement is plainly manifest. 

In this stage of development or metamorphosis, the cells are usually more or 
less elongated, though they often appear spherical. They have the power of chang- 
ing their shape, sometimes appearing very much elongated, at other times slightly 
oval, and then spherical. 

All of these forms are noticed frequently within a brief space of time, in the 
same cell, while watching its motion. 

The elongation is always in the direction in which the cell moves. Before 
the cell becomes active the hair-like appendage (cilium) cannot be seen, and in many 
instances after motion has commenced these processes are so fine that it is impossible 
to detect them, even by the best glasses. These cells contain a large central single 
or compound nucleus, around which are numerous minute spherical and oval granules 
or cells, many of which are in active motion. 

Those in active motion are probably sperm cells to these organisms, and the 
others germ cells. 

Following the stage of independent activity comes that of filamentous metamor- 
phosis. During this period the activity is slight, being confined to very slow, almost 
imperceptible, forward motion, which takes place at short intervals, or appears to be 
somewhat periodic. The hair-like projection becomes elongated and enlarged in 
calibre, and soon is seen to be a membranous tube. As this tube enlarges and 
elongates, the contents of the mucous cells (consisting of fluid and minute granules) 
pass into it, and the minute cells usually become arranged in a single moniliform 
row along its cavity, as seen at z, Fig. i, PI. I., d, e, 1, m and i, Fig. 7, Plate VI. 
As the contents of the mucous cell pass into the tubular filament, it (the cell) grows 
smaller and smaller till finally it entirely disappears, leaving simply the resultant 
filament.* 



* Here is described briefly an interesting organic process, one from which, when physiologically, or slowly and 
healthfully performed, emanate all the filaments of the muscular, fibrous and nerve tissues of the animal body, but which, 
when the metamorphosis is too hasty or rapid, becomes an abnormal action, resulting in a preponderance of solids, and, in 



l6 DIPHTHERIA AND SCARLET FEVER. 

Often two or more cells are united by one or more tubular filaments, i, m, Fig. 
7, PL VI., z, Fig. i, PI. I. 

Sometimes two or more filaments proceed from the same cell, as seen at 1, 
Fig. 7, PI. VI. The number of filaments is determined by the number of hair-like 
processes, and these are increased as the tendency to filamentous metamorphosis is 
increased beyond the normal standard. At m, two mucous cells have entirely emptied 
their minute cell contents into the connecting filaments. After the cells have disap- 
peared, we have simple filaments, as seen at p and q, Fig. 7, Plate VI. Often the 
mucous cells arrange themselves in moniliform rows, as at n and o, Fig. 7, Plate VI. 

r, are the minute cells and moniliform short filaments that make up the contents 
of the mucous cells. These are highly magnified. At the extremity of the forming 
filaments at g, Fig. 7, Plate VI., short, active, moniliform lines of minute cells and 
single cells are escaping. This has only been noticed in a few instances. 

u, spores of the saccharomycetes cerevisise, which occur through the mucous 
singly, and in short, branching, moniliform rows. 

s and t, highly refractive, oblate spheroidal cells of a pearly appearance, contain- 
ing bodies resembling spores, t, is an edge view and s, a side view. In the- right hand 
cell at s, are short filaments with the spores. The spores are of a reddish transparent 
orange color. 

Many of these cells are entirely empty. When mature they fracture from the 
circumference towards the center at numerous points, allowing the spore contents to 
escape. Thev are quite numerous in the exudations, and are the same as b and c, 
Fig. 8, PI. VII, in the urine. 

The expectoration and exudation in Scarlatina contain numerous confervoid fila- 
ments, like those at h, f, Fig. 6, PI. V. e, n, i, Fig. 8, PI. VII, of the urine of the 
same disease. 

Bloqd of Scarlatina. — The appearance of the abnormal bodies in the blood of 
Scarlatina Anginosa is so nearly identical with those seen under Diphtheria, Fig. 4, 
PL IV, that they will not require repetition here. 

Desquamated Cuticle of Scarlatina. — Dec. 19th. Placed about four grains of des- 
quamated cuticle from a Scarlatina patient in a watch glass, with a little pure water, 
tightly covered and set aside at a temperature of 65 Fahr. The dry cuticle was 
made up of flat, scale-like epithelial cells, each containing a" large central nucleus, sur- 
rounded by minute cells or granules. 

Twenty-four hours after the large central nuclei, s and s 1 , Fig. 9, PL VII, of 
the epithelial cells n and q, had taken an independent motion, and were moving about 
in the epithelial cells and escaping. 

After having escaped from the epithelial cells, the minute, hair-like appendages 
could be quite distinctly seen, as at a and b, Fig. 9, PL VII. 

The movements were very much more active than I had previously noticed in 
the epithelial cell products of mucous surfaces, c, represents the cells a and b, after 
the hair-like processes have begun to enlarge into a tubular filament. 

d, represents the spores of a miuute algoid vegetation, that have escaped from 
the flattened epithelium cells. These spores move independently in all directions. 

e, f, and k, represent these spores united into moniliform filaments. 

m, represents a blunt, tubular filament (algoid) with cells united in twos. 

g and h, represent short, algoid filaments with cells united in twos and threes, 
and the lines of demarcation between the individual cells obliterated. 

r, represents a long, algoid or fungoid filament, with no appearance of cross 
lines or cells. The inside cells have united into a uniform inside tube. 

All of these filaments have the power of independent motion. 

The motions are slow, and consist of the waving or vibrating of their extremi- 



consequence, congestions and exudations, the damming up of the capillary blood streams, checking and even stopping 
circulation locally, which may produce the pathological states of inflammation and gangrene. This subject will be more 
fully treated in another paper. 



DIPH JHKKIA AND SCARLET FEVICR 



ties — leptothrix ? 1, is a diatom from' the water drank, u, probably the urate of soda. 
x, crystal, probably phosphate of lime. 

Urine of Scarlet Fever. — Fig. 8, PI. VII, represents the various abnormal bodies 
found in the urine of Scarlatina, when the disease is at its height, a, b and e, rep- 
resent a peculiar kind of flattened, oblate spheroidal cells, containing orange-colored 
sporoid bodies, a and b, represent side views, and an edge view. They belong to 
the same class of bodies as s and t, v and w. Fig. 7, PI. VI. They occur frequently 
in the urine. 

d, represents cells from the parent epithelial cells of the bladder. They are 
single, and also aggregated in masses, and many of them manifest a disposition to 
filamentous metamorphosis, e, Fig. 8, PI. V, and f and g. Fig. 6, PI. V, algoid fila- 
ments, made up of an outside tube enclosing a moniliform line of minute spheroidal 
or oval cells, bearing a close resemblance to anabaina mollis. 

h, r, Fig. 6, PI. V, represent a species of leptothrix. Attached to the filament 
h, are a number of short ones, belonging to the genus anabaina. These short moni- 
liform filaments are the prevailing ones in Scarlatina urine, a single drop often con- 
taining many hundred, i, k and 1, Fig. 8, PI. VII, a species of hypheothrix which is 
quite frequently met with, o, large rhomboid crystals of lithic acid. These are quite 
abundant. 

w, Fig. 3, PI. I, a large, partially collapsed, membranous sack, resembling those 
found in the tomato or apple, and is probably accidentally present. Fig. 8, PI. VII, 
r, r, r, crystals of creatine. The crystalline forms s, t and n, are also sometimes met 
with. 

Some General Remarks Connected with the Pathology of Fevers, and the Tissues 
upon which Fever Poisons Primarily Act. — The first layer of cell organisms, through 
which food, medicinal agents and poisons have to pass in entering the animal bod}', 
is the epithelial. 

It is very evident that medicinal agents and poisons must act upon these cells, 
modifying their organizing and nutritive functions, and the derangement produced must 
first exist in these cells, and secondarily the more highly animalized elements and tis- 
sues beyond become affected, through the poisoned and medicated products furnished 
them by the epithelial tissue. 

There is hence evidence for believing that all febrile diseases, eruptive and other- 
wise, are intimately connected with functional and structural derangements of the cells 
of epithelial tissue. So intimate is the relation that these functional and structural 
derangements appear to constitute the disease. The different functional and structural 
disturbances of various portions of the epithelial structure would seem to give rise to 
the various types of fevers. The primary causes of these functional and structural 
derangements in most fevers are varied, numerous and obscure, while in others which 
are contagious they are more defined, each being excited only by a particular, specific 
cause. 

Before entering upon a few general remarks on the aetiology, etc., of fevers, indi- 
cated by microscopic investigations of the epithelial system in pyrexial states, I will 
briefly refer to some generally received views on these diseases. 

In primary fevers there is a general pyrexial state, without any evident patho- 
logical lesion, there being, to the unaided eye, no observable localized disease. 

As all organs and tissues appear to participate in the febrile action, when it is 
once established, its seat appears, and is supposed to be, no more in one tissue than 
in another. It has, however, been noticed that the first symptoms of the manifest 
invasion present themselves through the nervous system. 

It has therefore been supposed probable that the "fever poison" first invades 
the animal system through the channel of the nerves. These nerve symptoms, how- 
ever, will be shown further on to be probably but secondary results in the invasion. 

Cullen's definition of fever, modified by Christison, is as follows: "After a pre- 
liminary stage of languor, weakness and defective appetite, acceleration of the pulse. 



DIPHTHERIA AND SCARLET FEVER. 



increased heat, great debility of the limbs and disturbance of most of the functions 
without primary local disease." 

The great French anatomic schools, composed of able investigators, advanced a 
theory, which was generally entertained throughout Europe. 

This theory regarded fever as the "constitutional result, and its symptoms as 
the general expression throughout the system, of the effects of a localized process of 
disease, having for its constant seat a part of the intestinal canal." 

In fevers there is an increase of temperature above the natural standard of 
about 4° Fahr.; even during the algoid stage of the disease, the elevation of tempera- 
ture is present. 

This has been noticed to be a constant morbid condition of fevers. It is now 
generally admitted that the chief source of the increased temperature in fevers, arises 
from increased activity of the causes which operate in the production of the healthy 
temperature. 

The source of healthy animal heat is held to be developed by the nutrient 
changes perpetually going on in the tissues. 

An able enquirer — Virchow— assumes that the nutrient metamorphosis of the 
tissues is increased in fever, and as a natural and necessary consequence, this gives 
rise to increase of temperature. This nutrient metamorphosis consists of those organiz- 
ing changes going on both in nutrient materials supplied to the system, and those 
interstitial changes by which the constituents of the body themselves are metamor- 
phosed and removed. Virchow supposed that this increased metamorphosis was the 
consequence of some internal, excitant cause, the real nature of which is unknown. 

Lyon, in his work on fevers, p. 33, says: "Some facts determined by recent 
investigations and experiments would appear to show that the first steps in the 
establishment of febrile conditions are not to be sought for in the blood itself, or in 
any part ©f the circulating apparatus, but to indicate certain deranged conditions of 
the nervous system as more likely to furnish us with an explanation at once natural 
and proper on this point." Virchow believed that the elevation of animal temperature 
in fevers arose from a kind of paralytic condition of the nervous system. This is 
supposed to have been well established by numerous experiments. Becquerel, Brescher 
and Helmboltz, in experiments on that kind of nervous irritation which excites muscular 
contraction, found that it increased animal temperature. In opposition to this Bernard 
has proved that section of the sympathetic nerve in the neck is followed by rapid 
increase of temperature in the corresponding half of the head. Brown-Sequard's experi- 
ments are to the same effect. Weber has shown that the heart's action is arrested 
by the irritation of the vagi nerves. It has long been known that section of these 
nerves causes acceleration of the pulse. 

Ludwig and Hoffa have shown that in moderate irritation of the vagi, the 
lateral pressure of blood in the arteries is lessened; while Volkman and Towelin have 
determined that it increased after section of the nerves. Fraube has found that digitalis 
acts as as irritating stimulant upon the regulating nerves of the heart, and that a dimin- 
ished temperature is produced by it, which he attributes to the diminished velocity of the 
blood stream. 

From these experiments it has been inferred by authors "that the causes that 
regulate the velocity, tension and other physical conditions of the blood stream and the 
vessels which carry it, seem unquestionably to reside in the nervous system, which ex- 
ercises a sort of regulator or moderator function over the circulation, and through 
the circulation over the animal temperature." 

Cullen held that " the first link in chain of fever actions, was a depressed brain 
and nervous system." The spasm (or tonic contraction) of the capillaries, he con- 
sidered as resulting from the depression of the brain and nervous cehters, and that 
the reaction of the circulation was an effort to overcome this state of spasm of the 
extreme vessels. After the tissues have become once deranged by being nourished 
with abnormal food, organized by epithelial cells deranged in their functions, we 



DIPHTHERIA AND SCARLET FEVER. ig 

might well expect to find them in a diseased, irritated condition, which would mani- 
fest itself by a train of abnormal symptoms, which would continue until the exciting cause 
was removed. 

With regard to the elevation of animal heat, we would state in this connec- 
tion some few facts which go to show that animal heat may to a considerable extent 
be developed by the organizing processes of epithelial cells. After animal life has ceased, 
we have known the temperature of the body of a horse twelve hours after death (tem- 
perature of atmosphere 40 Fah.) to stand at 160 Fah. This high temperature arose mostly 
from the rapid organic changes going on in epithelial tissue, and from interstitial tissue 
dissolution. We have known the body of a dog, poisoned with veratrine, twelve hours 
after death to stand at 90° Fah. In the development of yeast cells in fermentation, 
the temperature of the fermenting mass often rises (where large masses of matter are fer- 
menting, to from 120 to 150 Fah. 

In the decay of nitrogenized tissues the temperature sometimes rises even above' 
150 Fah. 

In the rapid interstitial changes going on in fevers, we might well expect to find an 
elevated temperature of the animal body. 

After the phenomena noticed in the microscopic examinations of the epithelial cells 
in various parts of the epithelial structure, in health, during the period of febrile incuba- 
tion, and after the manifest invasion of the disease, there appears to be evidence for be- 
lieving that the nervous system is not the department of the organism first encroached 
upon, or the avenue through which the exciting cause of fever first passes, in invading 
the animal system. 

There is a cell structure making up a considerable portion of the organism, which 
possesses a life independent of the animal body, the cells of which vegetate and develop after 
animal vitality ceases, as has been fully shown in the preceding pages. 

This tissue is composed of cells, the function of which is to assimilate and 
organize the nutrient matters of the food into the various products which are de- 
signed to be appropriated in building up and nourishing the various tissues of the 
animal body. It is known by the name of epithelial tissue, and makes up the organ- 
izing portion of all glandular masses and surfaces. The cells of this tissue are extra- 
vascular, and so far as known, not supplied with nerves. All the external surfaces of, 
and avenues of approach to, the more highly animalized parts of the system are 
covered and guarded in all and every part by these epithelial cells. Nothing can 
enter the system without first passing through the cells of this assimilating and organ- 
izing epithelial envelope. This epithelial envelope is th^ ultimate basis of the entire 
organic structure. Its individual cells are the avenues and apparatus through which 
all the nutrient materials of the food have to pass, and be assimilated and organized, ere they 
are fitted to nourish and sustain the various tissues. 

The tissues themselves, outside of epithelial or glandular cells, have no power within 
themselves of organizing matter from blood for their support. The epithelial cells are 
the avenues through which alimentary, medicinal and morbific agents reach the system- 
ic tissues, and are the ultimate bases of many important physiological and patholog- 
ical processes. 

All febrile excitants must consequently act primarily upon the cells of this tissue, 
deranging -their organizing functions so as to impart abnormal properties to the matters 
organized. 

The period from the commencement of the action of the deranging influences 
upon these cells to the time when the abnormal organized products begin to produce 
perceptible derangements in the nerve and other tissues which these organized matters 
nourish, is the period of incubation. Of the different types of morbific agents which 
produce the different types of disease, each acts in its own peculiar way upon these 
cells of "extravascular life, producing in them specific changes in their organizing func- 
tions, which in each case results in a particular type of disease. 

This matter will be more fully set forth in a paper in progress on the "Ultimate 



DIPHTHERIA AND SCARLET FEVER. 



Structure and Functions of Epithelial (glandular) Tissue, and how Influenced in Function 
by Morbific Agents." 

It is through the cells of this tissue that most of our medicinal agents and poisons pro- 
duce their beneficial or baneful results. 

The study of the specific action of the various agents of the materia medica, etc., 
upon the gland cells, opens up a new and rich field for careful investigation, which will yet 
result in the discovery of ultimate organic actions and cardinal truths that will tend to reduce 
the healing art more to an exact science, and establish unvarying guides in many instances 
for the practitioner. It is in studying the functions of this primordial structure in health 
and disease, and under the influence of medicinal agents, that we may expect to find 
much that is new and true respecting those obscure ultimate physiological and patho- 
logical changes and medicinal effects which lie at the very foundation of medical science, 
and which are so important to understand in order to free the practice of medicine from an 
empiricism which has ever clung to it in defiance of past research. 

In fevers the organizing cells (epithelial) become dry, parched, and are so poisoned by 
morbific agents that their normal functions of organizing cells are much deranged, and to a 
great extent cease. 

Nutrient materials introduced into the stomach not being, save to a limited extent, 
assimilated and organized, act as foreign bodies, producing irritation of the intestinal canal 
and system generally. On the other hand, interstitial death and decay become rapid, pro- 
ducing debility, emaciation, etc. This state of things necessarily results in the long train of 
symptoms attendant upon fevers. 

The rapid interstitial changes are efforts on the part of nature to purge the system of 
morbific materials which have already been organized and become incorporated in the tissues 
during the period of incubation. This morbific matter must be disposed of or eliminated 
before recovery can take place. 

The .symptoms in any given case of fever are but the expressions of the extent to 
which the morbific poisoning has invaded the tissues, and of the efforts on the part of nature 
to rid the system of the poisoned epithelial products already appropriated, and the tendency 
to check the further organization of products for nutrient purposes, until the system becomes 
purged of the fever poison. This explains the reason why it is so useless to attempt to 
"break up" well-established fevers, except by removing or rendering inert the morbific cause. 
In pure fevers there are no perceptible organic lesions. The disease is one of function instead 
of structure. The primary seat of the derangement is in the ultimate epithelial cells, the 
very basement structure of the organism. In eruptive fevers the cutaneous surface becomes 
involved, and there is also a tendency for the mucous and serous surfaces to take on like 
pathological conditions. These fevers are distinguished from each other by the character of 
the surface lesions. In Scarlatina and measles there is a peculiar tendency for the mucous 
membranes to become involved. The former is commonly attended with a peculiar and char- 
acteristic form of sore throat (diphtheritic), while the latter is usually accompanied by a 
watery exudation from the eyes and nose (coryza), and a bronchial affection varying in extent 
and importance. 

In small-pox there is a tendency to lesion of the serous surfaces (the pleura especially), 
and occasionally the mucous coats of the intestines are involved (pustules on the mucous 
intestinal surfaces). 

In eruptive fevers and typhus, one attack gives a peculiar protective immunity against 
its recurrence in the same individual. The cause of this protective immunity may possibly 
be arrived at by carefully studying the changes impressed upon the ultimate epithelial cells 
by the specific causes of these diseases.* 

The spores of many algas and fungi, and perhaps other cryptogams, produce a febrile 
condition of the mucous lining of the air passages when inhaled. This febrile condition is 
local, and confined to the delicate parent epithelial cell surfaces with which the spores come 
in immediate contact. It often lasts from one to several hours after removal from exposure 



*The length of time that this impress of immunity lasts in any given case is determined by the length of the life and 
existence of the epithelial cells receiving the impress. Our epithelial cell envelope is constantly dying, disintegrating and 
disappearing, and new cells are formed to take their place, so that the integrity of the envelope is constantly preserved. 



9 



DIPHTHERIA AND SCARLET FEVER. 2 1 

to the morbific cause. In walking over, disturbing or pitching old, mouldy straw or hay, the 
throat, mouth and fauces become dry, hot and parched, and there is a constant desire to 
swallow, hawk and spit, with an almost entire suppression of the normal secretions of these 
surfaces. 

Verv soon this dry, congested sensation extends into and throughout the air passages 
of the lungs, and is there accompanied by a heavy, congested feeling. 

In walking over "peaty ague bogs," where the surface is broken, exposing the fresh 
soil covered with ague vegetation, during the months of July, August and September, or in 
passing through the heavy night air and vapors in malarial districts, the same or similar 
febrile sensations to those from mouldy straw and hay are experienced.* 

These sensations often last for hours, and sometimes during an entire day, after 
removal from the morbific cause. On examining the expectorated mucus, it is found filled 
with fungoid and algoid spores, and fragments of fungoid filaments. We have then here an 
exciting cause of local febrile excitement, which any one may be fully satisfied of by exposing 
himself to the condition just described. That the morbific poison in these cases is crypto- 
gamic, there is no possible doubt, as in hundreds of instances in our observations, where this 
febrile condition of the air passages has been excited, the expectorated mucus has been found 
to contain uniformly fungoid and algoid bodies in great numbers; and further, these bodies 
were the only foreign substances in the mucus that was constantly present in such cases. 

The atmosphere in certain localities, especially the heavy, damp, night atmosphere, is 
often found loaded, during the season of active cryptogamic development, with the invisible 
spores of numerous microscopic cryptogams, that multiply and develop with great prolific- 
ness, some upon living, some upon diseased, and others upon dead and decaying organic 
tissues. 

This established, we may go one step further and reasonably conclude that bodies 
which are capable of exciting local fever in the epithelial surfaces with which they come in 
contact, by a few minutes exposure to them, may, by frequent and long exposure of the sys- 
tem to the same cause, become so diffused throughout the organism by being inhaled and 
taken into it with the food and drink, as to communicate their morbific properties to the 
entire epithelial surfaces of the intestinal canal, and the lacteal, lymphatic, glandular and 
vascular epithelial surfaces, and so derange the functions of the organizing cells as to render 
the products organized by them, for the nourishment of the nervous and all other tissues of 
the body, poisonous. As soon as these poisoned nutrient products become appropriated' by 
the tissues, to a certain extent, the system gives way to those powerful efforts of nature, 
which are designed, not only to prevent as far as possible the further introduction of the fever 
poison, but, by rapid interstitial changes, eliminate from the organism the poisoned organized 
matters that have already been appropriated by the tissues during the period of incubation. 

The sum of these manifestations of nature constitutes the disease known as fever. 

These remarks apply to all fevers, and especially to those which are not regarded as 
contagious. In those that are contagious there are generally surface lesions in the shape of 
eruptions. In this class, called eruptive, the morbific cause is no doubt of a similar character 
to that of other fevers, but seems to possess in addition the peculiar property of those organ- 
isms known as "yeast plants," capable of multiplying almost infinitely in the animal system 
from a small beginning. The animal system to this vegetation seems to be a prolific "hot 
bed," in which they develop and multiply and extend without limit. They also possess the 
peculiar property of impressing upon the epithelial cell system the power of resisting to a 
remarkable extent subsequent invasions of the same disease. 

It has been, however, observed, that as the period lengthens from the time of the first 
invasion of the disease to subsequent exposures, the tendency becomes greater and greater, 
or the epithelial cell system has less and less power to resist a second invasion. 

This is an interesting field for inquiry. I will here suggest what appears to point 
in this direction, and which may be found on careful and extended research to be 
the true cause of this susceptibility to a second invasion. 

* That this local febrile excitement acts primarily upon the epithelial cells is evident from the fact that the first 
abnormal indication noticed is the suppression of the epithelial cell secretion ; the throat, fauces, bronchi and pulmonary 
membranes becoming dry, parched, etc. 



DIPHTHERIA AND SCARLET FEVER. 



The parent epithelial cells are to a considerable degree permanent and & inde- 
pendent organisms. Each has its attachment, and carries on its own organic processes, 
more or less independent of its neighbors. These parent cells are the bodies through 
which fever poisons gain access to the system. They are the bodies that are deranged 
in their organizing functions by fever poisons, and the organisms that must receive 
the more or less permanent prophylactic or resisting impress. This impress, upon any 
given epithelial cell, is no doubt permanent. It has been observed, and 1 have no 
doubt of its truth, that these parent epithelial organisms from time to time, and from 
a variety of causes, die, disintegrate and disappear, while new parent cells develop to 
take their place. 

In process of time, varying greatly in different persons, a great share of the 
original epithelial cell structures that had at some previous period received from an 
invasion of one of this class of diseases a protective impress, may have passed away, 
and a new system of epithelial cells taken their place. This new system of epithelial 
cells, having never been invaded, are, of course, like the first, susceptible of invasion, 
and in such case there would be a second attack of disease in the same individual. 
This attack would vary in intensity with the proportion of new epithelial cells in the 
glandular surface (each epithelial cell may be regarded to all intents and purposes 
a gland). If there are but few, the tendency to the second attack would be very 
slight — so slight that it would not be attended with any eruption, and with but slight 
febrile symptoms. 

This is what every physician has often noticed in his own case, when attending upon 
contagious fevers. 

I trust the investigations and few remarks here offered will interest the serious con- 
sideration of medical observers in this interesting field of inquiry. 

I am satisfied that careful observation of the epithelial cell organisms, the study in 
detail of their ultimate and all-important functions will not only be highly interesting 
to the observer, but will inspire him with that confidence he has seldom before felt, 
that his researches are now in the way of ultimate and important physiological and patho- 
logical truths, the solution of which has resisted past research, and which are destined to re- 
move many remnants of empiricism from the healing art, and reduce it more to a science of 
unvarying principles. 

It is only by the study in detail of this organizing cell system that we may expect 
to discover those primary and ultimate physiological and pathological actions and 
medicinal effects which lie at the very foundation of all healthy, diseased and curative 
processes. 

Resume. — The following is a brief summary of the facts and inferences which appear 
to be indicated by the foregoing investigations. 

ist. — That the disease occurring near Lancaster, Ohio, here described, and which 
proved so fatal, is Angina Maligna. 

2d. — That Angina Maligna is a contagious disease. 

3d. — That Angina Maligna is closely allied to Scarlatina Anginosa and that diphtheritic 
diseases generally are allied to those of the scarlatina type. 

4th. — That the primary seat of the disease in both Scarlatina and Diphtheria is the 
epithelial cells. That these are so deranged in their functions by the morbific cause df the 
disease, that the nutrient products which they organize become so poisoned that they 
poison the tissues they are designed to nourish. This poisoning takes place during the 
period of incubation. 

5th. — That morbific poisons cannot enter the system without first passing through and 
primarily deranging the epithelial cells and their products; as these cells envelop the entire 
organism, and guard all the approaches to it. That they affect the tissues by poisoning the 
organized matters which go to their support. 

6th. — That the epithelial cells of mucous and serous surfaces assimilate and organize 
all the nutrient matters which go to build up and support the tissues. 



DIPHTHERIA AND SCARLET FEVER. 23 

7th. — That the perceptible symptoms of the diseases are but expressions of the efforts 
of nature to eliminate from the system the morbific poison. 

8th. — That the exudations of the mucous surfaces in Diphtheria are produced 
by the too rapid metamorphosis of mucous cells into filaments, which filaments be- 
come woven together, forming a felt-like membrane, before they are fully liberated from the 
follicles. 

9th. — That the tendency to filament metamorphosis in Diphtheria is general through- 
out the epithelial system showing that it is a systemic disease. 

10th. — That the Mucor Malignans appear to be the primary cause of Angina Maligna, 
and of Angina Membranacea. That the diseases are specifically the same, the difference be- 
ing caused by the state of the system in the person attacked. 

nth. — That as the tendency is for the cells to become developed into filaments and 
resultant membranes before they are fairly out of the follicles, the object of any treatment 
should be to retard this filamentous development and promote the secretions, so that the cells 
may escape before they become filaments, also to check the development and to destroy the 
fungoid cause. 

12th. — When the filaments are strong and membranes tough and adhesive, mercurials 
should be resorted to, to soften the threads and render exudation less adhesive. 

13th. — That these diseases are but the efforts of nature to eradicate from the system 
morbific matters, that it should be the constant care of the physician not to run counter 
to nature in the efforts to cure the vitiated condition of the organism, but simply 
to endeavor to destroy the cause, and so to equalize, aid and modify her ac- 
tions as to alleviate suffering, facilitate her processes, and guard against dangerous 
results. 

14th. — That it is a normal action for the cell products of epithelial cells to become 
gradually metamorphosed into filaments. 

15th. — That if by any cause the metamorphosis prematurely commences and the pro- 
cess is accelerated, it becomes a pathological action, which tends to result in grave abnormal 
conditions. In epithelial tissue there result membranes, exudations, and clots; in connective 
tissue, the various cancerous and fibrous growths. 

1 6th. — That the epithelial cells have a life independent of the animal, all the external 
and internal surfaces of which they envelop, and protect. 

17th. — That they appear to be the primary seat of the functional derangements in all 
true fevers. 

1 8th. — That they are the probable organisms which receive the protective immunity 
by one attack of certain contagious diseases, that tends to guard the system against a second 
invasion of the same. 

19th. — That in health it would seem that neither nutrient, medicinal nor morbific 
agents can enter the system so as to nourish, medicate or vitiate the tissues of the organism, 
without first passing through the cells, and imparting a primary influence to them and the 
products they organize. 

20th. — That it is probable that morbific matters poison the tissues of the body through 
the nutrient products organized for their support by the epithelial cells. 

21st. — That local fever of the mucous surfaces may be excited at will by exposing 
them for a few minutes to contact with the spores of certain algae and fungi that develop 
upontague bogs, old straw, etc. 

2 2d. — That it is probable that by continued exposure to these and similar causes (the 
taking of spores into the system through the food eaten and the air inhaled), that febrile 
action over the entire epithelial surfaces, including those of the lacteal and lymphatic systems, 
would be excited, in which case general fever would result. 

23d. — That the action of the "fever poison" upon the nervous system is through the 
nutrient nerve products organized by the vitiated and functionally deranged epithelial cells, 
and hence is a secondary process or manifest symptom of the primary functional derange- 
ments of these epithelial cell organisms, or of the ultimate disease. 

24th. — That the treatment should be prompt and direct, aimed not only at the destruc- 



24 DIPHTHERIA AND SCARLET FEVER. 

tion of the cause, but at the removal of all the pathological conditions and states which this 
cause has excited. 

The Mucor Malignans should be checked in its development and destroyed, and at 
the same time the toughness and adhesiveness of the exudations should be softened, the 
choking and suffocation should be relieved, and the throat, fauces and air passages be kept 
in as comfortable a state as possible. To destroy the cause, quinia sulphate — all things con- 
sidered — is the best and most reliable remedy, as it braces up the enfeebled system while it is 
destroying the fungus. 

It is not enough to give it every two hours or every hour, but it should be admin- 
isted every half hour, and in some instances perhaps even oftener. It should be given in 
powder, so as to keep the throat and fauces constantly covered with it, and if necessary it 
should be snuffed and inhaled into the air passages. To destroy the toughness of the filaments 
and the adhesiveness of the membranes, small doses of mercurial often repeated are useful. 
To relieve the choking and suffocation, the simple hop poultice, applied as hot as it can be 
borne around the neck, and so covered as to allow the steam from it to be inhaled, is a very 
effectual relief. Also small doses of sulphuric ether in coffee, or the inhaling of a few drops 
of nitrite of amyl, may prevent sudden suffocation in cases where the physician is called 
in the last stages, and through these precious time may be gained for using vigorously the 
quinine. 

In conclusion, I take pleasure in expressing my obligations to Drs. Boestler, Efhner 
and Lewis, who have felt interest in my labors, and to whom I am indebted for much excel- 
lent material in these examinations. 

9 -West 29th St., June, 1882. 



PLATE I— FIG. i. 

{Amplification 2500 Diameters and over.) 

Forms found in the expectoration and exudations of diphtheria. 

A-S-T — Healthy buccal mucous corpuscles, page 9. 

B-C-H-l — -Mucous corpuscles from Amos Bear's mouth, showing the spinning of 
filaments in diphtheria. 

, D-E-M-page 9 — Mucous cells connected with filaments. 

E — A row of mucous cells. 

F — Mucbus cells spun into a long branched filament. 

G — Sporangia of Sphasrotheca Pyra — found also in pear blight. 

H-I-K-M-N-0 — Mucous cells from Nancy Bear, page 10. 

U — Automobile microspores — the bacteria and micrococci of authors. 

P — Microspores found in Q. and R. 

Q-R — Exuded Membrane in Diphtheria. 

W — Membranous vegetable sac found in urine of scarlet fever, placed here for con- 
venience. 

Z — Three cells in active filamentation. 



PLATE I. 




PLATE II— FIG. 2. 

Fodies found in the diphtheritic sloughs from the throat of Amos Bear. 
A-Embryonal form of diphtheritic vegetation-the bacteria and micrococa of 

writers — page 10. 
B^C-D— Mature mycelial filaments, running in all directions through the sloughs. 
E-F-G r H— Spores and microspores of the Mucur Malignans. 

I — Ascus. 

K-P— Sporidia of pear blight— Spheerotheca Pyra. 

M-N-0 — Sporidia with mycelial filaments do. 

U-V-W— Large mucous cells infected with entophytic fungi Mucor Malignans, 
pages 10 and 1 1. 



PLATE II. 




PLATE III— FIG. 3. 

The mature plant of diphtheria developed by culture, page 11. 

Mucor Malignans. — A — Fertile plant of Mucor Malignans with three clusters of 

sporangia. 

C 

B — Plant with erect filament and undeveloped fruit. 

C-D-E — Stroma or membranous net work of mycelial filaments dotted over with 
microspores. 

W — Microspores that fill the sporangia at A. 

G-M-N-S-T — Automobile spores, some arranged into filaments. 

U — Collection of mature sporangia and filaments matted together as in the mem- 
brane. 

V — Separate mature sporangia. 



PLATE III. 



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PLATE IV-FIG. 4. 

Abnormal morphological elements found in the blood of Diphtheria and Scarlet 
fever. 

A-B — Masses of colorless corpuscles filled with embryonal forms (spores) of the 
Mucor Malignans. 

C-C — Amoeboid projections of protoplasm do. do. 

D — Automobile microspores more highly magnified. 

E — Caudate cells like I and B, Fig. 1, PI. 1. 

F — Endothelia of blood vessel with entophytal vegetation escaping. 

G — A large endothelium forming into a filament. « 

H and K — Skeins of mycelial filaments in the blood. Abundant in Amos Bear's case. 

M-N — Fibrin masses enclosing mycelial filaments. 

I — Filament resembling neurine, page 13. 

FIG. 5. 

Crystalline bodies found in the urine of Scarlet fever and Diphtheria. 

A-B-C-D— Uric acid. 

E-K — Peculiar forms do. 

I — Urates of soda and ammonium. 



PLATE IV. 




PLATE V-FIG. 6. 

Forms found in urine and sputa of Scarlet fever and Diphtheria. 

A — Anguillila aceti from vinegar gargle of Amos Bear. 

B — Mycelial filaments found in sputa of diphtheria. 

C — A knot ot mycelial filaments such as are found scattered over the membranes 
of angina malignans. 

F-G — Filaments from urine of scarlet fever. 

H — Leptothrix with anabaina. 

M and M 1 — Structureless mycelial filaments — -urine of diphtheria. 

Q-Q 1 — Cells uniting to form filaments. 

R — Vibriones so-called. 

L-S-T-U-V-W — Embryonal spores and filaments more highly magnified — the 
bacteria and micrococci of authors. 

X — Mycelial filaments such as also occurred in vast numbers in ripe persimmons in 
Ohio, 1862. 



PLATE V. 




* 'I 



PLATE VI-FIG. 7. 



Bodies found in the expectoration and exudation of Scarlatina Maligna. 

A — Normal mucous cell. 

B-C-H — Mucous cells in an active state. 

D— E— L— M— I — Do. do. in active filamentation. See also Z, Fig. 1. i late 1. 

C — Mucous cell with micrococci spores escaping; at end of filament. 

N near A — Mucous cells arranging- themselves into rows to form filaments. 

O— Do. do. 

P-Q — Mycelial filaments of Mucor Malignans. 

R — Moniliform filaments formed and forming. 

S and T — Highly refractive spheroidal cells of reddish orange color; filaments in eel 
on right. 

U — Alcholic yeast. 

V'-W — Cells shedding contents. 

V-X-V-Z-N near Z — Contents more highly magnified. 



PLATE VI. 




PLATE VII— FIG. 8. 

Bodies found in urine of Scarlet fever. 

A-B-C — Sporangia of Mucor Malignans. 

D — Parent epithelial cells from bladder. 

E — Mycelial filament. 

I-K-L-N near B — Species of hypheothrix, 

O — Uric acid. 

R-R-R — Creatine. 

S-T-N near R — Other forms of uric acid. 

FIG. 9. 

Scarlet fever. 

A-B-C — Dermal epithelia cultivated. 

D — Micrococcus spores from epithelium. 

E-F-K — Ditto, united in moniliform filaments 

G-H — Ditto, united by twos and threes. 

L — Diatom from drinking water. 

M — Filament of spores united by twos. 

N-Q — Epithelial cells of skin of Scarlet fever. 

O-P — Abnormal sporangia of Mucor Malignans, both broken. 

R — Long tubular mycelial filament. All these were automobile like oscfllatoriacae. 

S-S — Central nuclei of N and Q. 

T — Patch of membrane with mycelial filaments of Mucor Malignans curiously 
twisted together and curled. 

U — Urate of soda. 

W — Barb of feather. 

X — Phosphate of lime. 

Y — Patch of membrane. 



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